By means of external electrical stimulation the nature of the muscular activity associated with movements of the schistosome has been examined. In these experiments a suction pipett was used for delivery of current pulses to the posterior dorsal surface of male schistosomes and resultant changes were recorded. Both hyperpolarizing and depolarizing responses are dependent on external calcium. The responsiveness of the worm to stimulation is decreased by Mn++, Ca++, or La+++. Dopamine and 5-hydroxytryptamine have little effect on the response to stimulation, but carbachol depresses both depolarizing and hyperpolarizing responses. Basic studies on electrical potentials recorded from male schistosomes have been completed and it appears that these potentials arise in the tegument of the parasite. Tegumental potential is unaffected by altered concentrations of either calcium or chloride but lowering the external sodium concentration does depolarize the tegumental membrane. Potassium causes marked depolarization of this membrane potential. These results might be expected if there is a significant active transport component contributing to the tegumental potential. D-600, a calcium antagonist, blocks the potassium-induced contraction. This result indicated that external calcium is needed to maintain the potassium contracture and movement of calcium from external medium into parasite appears to be triggered by depolarization of the tegumental membrane. Praziquantel, a new antischistosomal drug causes massive contraction of the parasite's musculature. This contraction is dependent upon external calcium ions in the incubation medium surrounding the parasite. Praziquantel-induced contracture of the parasite's musculature is not blocked by D-600. Praziquantel induces a rapid uptake of radio-labeled calcium from the incubation medium. The route by which praziquantel induces its rapid tension increase is not by way of depolarization, but rather by way of some change in ionic permeability of the tegumental membrane to calcium.